自发性椎动脉夹层（sVAD）的病因和进展机制尚不完全明确，也无有效预测手段。前期工作中课题组在国际上率先发现椎动脉发育不良（VAH）是导致sVAD的重要原因，但其机制尚未阐明。已有的研究发现VAH的解剖异常可引起血流动力学改变，而血流环境改变是促发sVAD的危险因素之一。但两者的确切联系未见报道。主要研究瓶颈在于VAH难以进行动物模型的构建，而单纯的在体数字模拟对于类似VAH的非均一性管腔的建模也有非常大的局限性。本课题组则依托在3D生物打印技术上的优势，率先通过构建个体化的“仿真”VAH模型和sVAD模型，考察体外循环状况下发育不良血管内流体速度、流量分布、压力及壁面切应力信息，以几何多尺度方法进行拓扑拟合，探讨同sVAD血流动力学结果之间的相关性，从而阐明VAH所致血流动力学异常在sVAD发病中的作用。本课题将有助于进一步加深我们对sVAD的认识，为评估其发生发展提供量化的依据。

The etiology and the mechanism of disease progression in spontaneous vertebral artery dissection (sVAD) is not entirely clear still now, and there is no effective way to predict this disease. In our previous work, we found for the first time, that vertebral artery hypoplasia (VAH) is a potential risk factor for sVAD and that these two conditions tend to be ipsilaterally associated. Current studies have indicated that anatomical abnormalities in VAH can result in hemodynamic changes, which is one of the most important risk factors for sVAD. Based on these evidences, we hypothesize that VAH can lead to sVAD by altering hemodynamic. However, this mechanism is never researched before. The main bottleneck is difficult to build VAH animal models in vivo, in addition, simple noninvasive ways to detect the blood flow for VAH may have many limitations. We have established some in vitro blood vessel model by 3D bio-printing technology before. In this research, we plan to further our study to construct a in vitro model of VAH and sVAD by 3D bio-printing way. Then we will use particle image velocimetry to obtain ComPutational fluid dynamies numerical simulationd method to obtain the fluid velocity , flow distribution, pressure and wall shear stress information of these model. Moreover, its association with hemodynamic results of sVAD model will also be analysed. Our result may form an important basis for a better understanding in the pathophysiology of sVAD, and eventually provide the rationale for a novel strategy to prevent of the disease.